The metabolic syndrome is a cluster of disorders that includes obesity, hypertriglyceridemia, hypertension, non-alcoholic fatty liver disease (NAFLD), impaired glucose metabolism, and insulin resistance all of which contribute to increased risk for the development of diabetes and cardiovascular disease1-4. The concept of a metabolic syndrome was popularized by Gerald Reaven in the 1980s who postulated that a common pathogenic mechanism must lay at the heart of these diverse conditions by demonstrating that a single dietary intervention, high-fructose feeding, can reproduce all the features of the syndrome in rodents5. Epidemiologic data indicate that increased sugar consumption is a major contributor to the development of the metabolic syndrome including obesity and diabetes6. Increased consumption of sugar-sweetened beverages accounts for the majority of the increase in sugar ingestion7. Sugar is a disaccharide composed of one glucose and one fructose molecule. The fructose component of sugar is particularly harmful. Prospective clinical experiments demonstrate that increased fructose ingestion, but not increased glucose ingestion, promotes dyslipidemia, increases visceral adiposity, and impairs insulin sensitivity in human subjects8. Studies also suggest that increased sugar or fructose consumption also contributes to the development of Non-Alcoholic Fatty Liver Disease (NAFLD)9. The mechanisms by which high-sugar or high-fructose feeding cause metabolic dysfunction remain unclear. Furthermore a specific, quantifiable acute biologic response to fructose ingestion has never been defined.
In view of the prevalence of metabolic syndrome and associated disorders of metabolism, the role of fructose in the development or complications of these disorders, and the absence of a specific quantifiable biologic response to fructose ingestion, a need exists for methods of monitoring the fructose response in a subject.